Xiaoliang Fu1, Wei Zhang1, Yansheng Su2, Lu Lu3, Dong Wang1, He Wang1. 1. Departmentof Urology, Xi'an Tangdu Hospital, The Fourth Military Medical University, Xi'an, China. 2. The Chinese People's Liberation Army 323 hospital, Xi'an, China. 3. Armed Police Hospital of Shaanxi, Xi'an, China.
Abstract
BACKGROUND: It is known that microRNAs (miRNAs) are a class of small, non-coding RNAs that act as key regulators in various physiological and pathological processes. However, the regulatory mechanisms involving miRNAs in prostate cancer remain largely unknown. Here, we found that miR-103 is down-regulated in prostate cancer and closely associated with tumor proliferation and migration. Our objective was to explore the role of the miR-103 in prostate cancer. METHODS: In this study, we measured miR-103 level using real-time polymerase chain reaction in the human prostate cancer cell lines, including PC-3, LNCap, 22Rv1, DU145, and the normal prostate epithelium cell line RWPE-1, a total of 25 pairs of primary prostate cancer tissues and adjacent non-cancerous tissues (NCTs) were measured also. In addition, over-expression of miR-103 in prostate cancer cell lines to determine the role of miR-103 in prostate cancer. RESULTS: We found that miR-103 is down-regulated in prostate cancer and closely associated with tumor proliferation and migration. In addition, over-expression of miR-103 apparently inhibits prostate cancer cell proliferation and migration in vitro. Gain-of-function in vitro experiments further show that miR-103 mimics significantly inhibited prostate cancer cell proliferation, invasion and increase the cell cycle in G1 phase, while promoted cell apoptosis. Subsequent dual-luciferase reporter assay identified one of the proto-oncogene PDCD10 as direct target of miR-103. CONCLUSIONS: Therefore, our data collectively demonstrate that miR-103 is a proto-oncogene miRNA that can suppress prostate cancer proliferation and migration by down-regulating the oncogene PDCD10, indicating that miR-103 may represent a new potential diagnostic and therapeutic target for prostate cancer treatment.
BACKGROUND: It is known that microRNAs (miRNAs) are a class of small, non-coding RNAs that act as key regulators in various physiological and pathological processes. However, the regulatory mechanisms involving miRNAs in prostate cancer remain largely unknown. Here, we found that miR-103 is down-regulated in prostate cancer and closely associated with tumor proliferation and migration. Our objective was to explore the role of the miR-103 in prostate cancer. METHODS: In this study, we measured miR-103 level using real-time polymerase chain reaction in the humanprostate cancer cell lines, including PC-3, LNCap, 22Rv1, DU145, and the normal prostate epithelium cell line RWPE-1, a total of 25 pairs of primary prostate cancer tissues and adjacent non-cancerous tissues (NCTs) were measured also. In addition, over-expression of miR-103 in prostate cancer cell lines to determine the role of miR-103 in prostate cancer. RESULTS: We found that miR-103 is down-regulated in prostate cancer and closely associated with tumor proliferation and migration. In addition, over-expression of miR-103 apparently inhibits prostate cancer cell proliferation and migration in vitro. Gain-of-function in vitro experiments further show that miR-103 mimics significantly inhibited prostate cancer cell proliferation, invasion and increase the cell cycle in G1 phase, while promoted cell apoptosis. Subsequent dual-luciferase reporter assay identified one of the proto-oncogene PDCD10 as direct target of miR-103. CONCLUSIONS: Therefore, our data collectively demonstrate that miR-103 is a proto-oncogene miRNA that can suppress prostate cancer proliferation and migration by down-regulating the oncogene PDCD10, indicating that miR-103 may represent a new potential diagnostic and therapeutic target for prostate cancer treatment.
Authors: Anthony Monteforte; Brian Lam; Michael B Sherman; Kayla Henderson; Andrew D Sligar; Adrianne Spencer; Brian Tang; Andrew K Dunn; Aaron B Baker Journal: Tissue Eng Part A Date: 2017-11 Impact factor: 3.845